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. 2008 Nov;201(1):217-24.
doi: 10.1016/j.atherosclerosis.2007.12.058. Epub 2008 Mar 4.

Relation of smoking status to a panel of inflammatory markers: the framingham offspring

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Relation of smoking status to a panel of inflammatory markers: the framingham offspring

Yamini S Levitzky et al. Atherosclerosis. 2008 Nov.

Abstract

Aims: We sought to investigate the hypothesis that smoking is accompanied by systemic inflammation.

Methods and results: We examined the relation of smoking to 11 systemic inflammatory markers in Framingham Study participants (n=2944, mean age 60 years, 55% women, 12% ethnic minorities) examined from 1998-2001. The cohort was divided into never (n=1149), former (n=1424), and current smokers with last cigarette >6h (n=134) or < or =6h (n=237) prior to phlebotomy. In multivariable-adjusted models there were significant overall between-smoking group differences (defined as p<0.0045 to account for multiple testing) for every inflammatory marker tested, except for serum CD40 ligand (CD40L), myeloperoxidase (MPO) and tumor necrosis factor receptor-2 (TNFR2). With multivariable-adjustment, pair-wise comparisons with never smokers revealed that former smokers had significantly lower concentrations of plasma CD40L (p<0.0001) and higher concentrations of (CRP) C-reactive protein (p=0.002).

Conclusions: As opposed to never smokers, those with acute cigarette smoke exposure (< or =6h) had significantly higher concentrations of all markers (p<0.0001) except serum CD40L, MPO, and TNFR2; plasma CD40L were significantly lower. Compared with never smokers, cigarette smokers have significantly elevated concentrations of most circulating inflammatory markers, consistent with the hypothesis that smoking is associated with a systemic inflammatory state.

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Figures

Figure 1
Figure 1
Estimated mean differences (with standard error bars) for smoking categories versus referent never smokers for standardized log marker concentrations Zero represents no difference between smoking category and never smokers.

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